13.
Aldosterone
• Secreted by the adrenal glands in response
to angiotensin II or high potassium
• Acts in distal nephron to increase resorption
of Na+ and Cl- and the secretion of K+ and
H+
• NaCl resorption causes passive retention of
H2O

14.
Anti-Diuretic Hormone (ADH)
• Osmoreceptors in the brain (hypothalamus) sense
Na+ concentration of blood.
• High Na+ (blood is highly concentrated) stimulates
posterior pituitary to secrete ADH.
• ADH upregulates water channels on the collecting
ducts of the nephrons in the kidneys.
• This leads to increased water resorption and
decrease in Na concentration by dilution

16.
• Pregnancy induces increased synthesis of prostaglandin E2 (PGE2) which
inhibits ureteral peristalsis and may be responsible for the hypomotility
and distension.
• Increased oestrogen and progesterone production causes muscular and
hypertrophic changes in the urinary tract resulting in hypomotility of the
urinary tract.
• Increased production of chorionic growth hormone may cause some
renal hypertrophy.
• Mechanical obstruction by the enlarged uterus can contribute to
ureteral distension as well as changes to surrounding structures.

17.
Functional Changes
• Early in pregnancy increased RBF, secondary to increased CO and
renal vasodilatation
• This has been shown to be up to 40% above nongravid values.
• Usually a decrease in systolic pressure is seen, due to the decrease in
vascular resistance from vasodilation.
• This increased RBF  increased glomerular filtration rate (GFR). This
begins during the first few weeks after conception, is at its greatest at
the beginning of the 2nd
trimester and remains until after delivery.
• Creatinine, urea and uric acid clearances increase, therefore serum
levels decrease during pregnancy.

18.
• Acid base regulation altered decrease in the bicarbonate threshold. Early morning
urine specimen is more alkaline.
• Pregnant women tend to hyperventilate and subsequently mild alkalosis is often
present.
• Glucose, water-soluble vitamins, protein and amino acids are excreted during normal
pregnancy (increase in GFR  filtered load of nutrients to surpass the reabsorptive
capacity of the kidney, therefore these substances spill into the urine)
• Intermittent glycosuria is normal and makes screening for diabetes more difficult.
• Volume regulation ch.  gradual accumulation and retention of water and sodium.
• Most healthy women gain an average of 12.5 kilograms and most of this is fluid.
• The plasma volume doubles and this results in a fall in the plasma sodium
concentration (dilution).

19.
• Osmolarity levels decrease  stimulate a diuresis by suppressing ADH.
However, in pregnancy this does not appear to happen.
• It appears as though the osmoreceptors are ‘reset’ at a lower level to
avoid a continuous diuresis.
• Mean BP decreases by around 10 mmHg in early pregnancy  decrease in
peripheral vascular resistance; effects of progesterone (smooth muscle
relaxant).
• Renin concentration is 5 - 10 times greater in pregnancy, however the
pregnant women is extremely resistant to the vasoconstriction effects of
angiotensin II. Related to elevated levels of aminopeptidase which
destroys angiotensin II.
• Erythropoietic activity increases during pregnancy. This is possibly due to
an increase in erythropoietin levels from an increase in renal tissue

32.
How CKD should be managed in
pregnancy?
• All women with chronic kidney disease should be referred early in
pregnancy to an obstetrician and other specialist as necessary, to plan
subsequent antenatal care.
• However, with a few exceptions, the most important aspects of managing
chronic kidney disease in pregnancy relate to managing associated clinical
features, rather than the type of kidney disease.
• Regular monitoring of maternal renal function (serum creatinine and
serum urea), blood pressure, midstream urine (for infection), proteinuria,
and when appropriate ultrasound (to detect urological obstruction) should
identify pathological changes and allow timely intervention to optimise
perinatal outcome and maternal renal outcome.

33.
Before pregnancy:
• Ideally, all women with chronic kidney disease should be made aware of the risks
to their long term renal function and to the fetus before they conceive.
• Women with chronic kidney disease often have amenorrhoea but may still
occasionally ovulate and thus conceive.
• Contraceptive measures that consider clinical comorbidities should be taken by
those who do not wish to become pregnant.
• Folic acid 400 μg daily should be given as usual before conception until 12 weeks’
gestation.
• Low dose aspirin (50-150 mg/day) should be started in early pregnancy to reduce
the risk of pre-eclampsia and improve perinatal outcome.
• Fetotoxic drugs—such as ACE inhibitors and angiotensin II receptor blockers—
should be stopped before pregnancy if equally effective drugs are available, or as
soon as pregnancy is confirmed, if they are thought to be important for protecting
maternal renal function.